Scenario Walkthrough: Rural Polytrauma (TBI + Hemorrhagic Shock)
CLINICAL INTERVENTIONS & ROAD WISDOM
Step-by-step procedural execution with tactical field rationale for Case 01 under dark, rainy ground-unit conditions.
STEP 1: CIRCULATION PRIORITY
CDST P. 6, 8, 9 & 28Tactical field execution
Universal Initial Action (Pages 6 & 28) Basic Life Support Cadres (BAA vs. Registered ECA)
Both cadres immediately apply direct pressure to the compound femoral bleed, pack with hemostatic gauze, and apply a mechanical tourniquet 5–7 cm proximal until spurting halts completely. Apply pelvic sheet/binder.
If your crew is a Legacy BAA
Ceiling (Annexure A, Page 3): BAA cannot insert an IV line and cannot administer IV fluid therapy.
The Problem: External bleed controlled, but patient remains in hypovolemic shock (BP 78/42, HR 138) from occult internal abdominal bleeding. BAA cannot treat central hypovolemia.
🚨 BAA Backup Trigger: Radio dispatch immediately: "Priority 1 trauma with occult internal hemorrhage and shock. BAA crew unable to cannulate. Requesting immediate ILS/ALS intercept on R61 while we transport."
If your crew is a Registered ECA (Higher Certificate):
Capabilities (Annexure A, Page 3 & CDST Page 29): *ECA* CAN insert a peripheral IV line (>1 year old), CAN insert an adult IO needle, and CAN initiate conservative crystalloid fluid boluses (100–250 mL IV, titrated to maintain radial pulse or MAP ≥ 65 mmHg).
The Real *ECA* Ceiling (Annexure A, Page 10 & CDST Page 9): *ECA* cannot administer Tranexamic Acid (TXA) (Orange text: ^ANT^/~ECP~ only) and cannot run inotropes/Adrenaline infusions.
🚨 *ECA* Backup Trigger: Pumping liters of crystalloids causes the lethal triad (dilutional coagulopathy, acidosis, hypothermia).
Action: *ECA* establishes IV line, runs conservative 250mL bolus, and calls dispatch for ALS/~ECP~ intercept specifically for IV Tranexamic Acid (TXA) and inotropic support while en route.
Tranexamic Acid (TXA)(Antifibrinolytic Agent (Cyklokapron))
Adrenaline (Epinephrine) Inotrope / Push-Dose(Sympathomimetic Catecholamine)
Clinical Execution on Scene (CDST Pages 8, 9 & 29 | Annexure A): Intermediate & Mid-Tier Cadres (ECA & AEA)
Vascular Access: Both cadres initiate peripheral IV access (14G/16G) in limbs/hands for patients >1 year old.
*ECA* Specific Advantage: Holds scope for Adult Intraosseous (IO) insertion if peripheral access fails.
Damage Control Fluid Titration: Administer conservative, warm crystalloid boluses of 100–250 mL IV. Recheck vitals every 10 minutes, titrating strictly to maintain a palpable radial pulse (target SBP ≥ 90 mmHg or MAP ≥ 65 mmHg) to prevent dislodging forming clots ("popping the clot").
🚨 THE SHARED ECA / AEA BACKUP TRIGGER:
The Problem: Despite IV/IO access and conservative fluid challenges, the patient has active internal bleeding and remains in refractory shock (SBP 78/42, HR 138).
The Clinical Ceiling: Neither the *ECA* nor the *AEA* can administer Tranexamic Acid (TXA) or Inotropic / Adrenaline Infusions (both marked as ^ Orange text ^ on Pages 9 & 29: ^ANT^/~ECP~ scope only).
The "Why" for Students: Pumping liters of crystalloids does not carry oxygen and actively washes out clotting factors. The patient needs TXA to halt clot breakdown (hyperfibrinolysis) and inotropic vasopressors to maintain organ perfusion.
🚨🚨🚨The Radio Action: *ECA*/*AEA* initiates rapid transport immediately while radioing for an ALS/~ECP~ intercept rendezvous: "Priority 1 polytrauma with active internal hemorrhage and refractory shock. IV access established, conservative fluids running. Requesting ALS intercept for IV Tranexamic Acid (TXA) and inotropic support en route."
Advanced Life Support & Specialist Scope (ANT / ECP)
What the ~ECP~ Delivers Upon Intercept:
Antifibrinolytic Therapy: Administers Tranexamic Acid (TXA) 2g IV over 10 minutes (Orange text, Page 29) to stabilize clot structure within the critical 3-hour post-injury window.
Chemical Hemodynamic Support: Prepares push-dose Adrenaline (5–20 mcg boluses) or titrates an Adrenaline IV infusion at 2–10 mcg/min (starting at 5 mL/hr, Page 9) to maintain MAP ≥ 65 mmHg without volume-overloading the bleeding patient.
Point-of-Care Ultrasound: Performs an on-scene eFAST exam (Page 29) to directly visualize free fluid in Morison’s pouch and the pelvis, pre-alerting the receiving regional hospital to activate the surgical trauma team and uncrossmatched blood products prior to ambulance arrival.
THE OCCULT SHOCK TRAP
External extremity hemorrhage is arrested, yet vitals reflect worsening Class IV hemorrhagic shock: BP 78/42 (MAP 54) and HR 138. Do not assume stability. Concealed intra-abdominal / retroperitoneal bleeding continues unabated.
Vascular Access in Crashing Trauma
Resus PearlsTactical Road Wisdom
The Priority Check: Is the IV Line More Important Than the Occult Bleed?
The Clinical "BP Cuff Trick" for Collapsed Veins:
Palpation over Visualization: Know Your Anatomical Landmarks:
STEP2:Airway Compromise & The Crashing Brain
CDST P. 7, 10-14Tactical field execution
Basic Life Support Cadres (BAA vs. Registered ECA)
Execution (Pages 7 & 10): Manual in-line C-spine stabilization (jaw thrust, no head-tilt), rigid Yankauer suctioning of blood/vomitus, and gentle BVM ventilation at 1 breath every 5 seconds with 15 L/min O2.
Ceiling & Scope Trap: An OPA does not protect the trachea against pulmonary aspiration of blood and stomach acid. If the patient has trismus or intact reflexes, an OPA triggers vomiting. An *ECA* can only place an SGA in cardiac arrest (Annexure A Page 1).
🚨 BLS Backup Trigger: GCS ≤ 8 patient with intact reflexes or trismus who cannot protect their own airway. Action: Maintain basic BVM ventilations, keep airway suctioned, and call dispatch immediately for an ~ECP~ rendezvous to perform Rapid Sequence Intubation (RSI).
Intermediate & Technician Cadres (AEA / ECT / ANT)
Execution (CDST Page 11): Assess for presence of gag reflex:
If gag reflex absent: *ECT*/^ANT^ can insert a Supraglottic Airway (SGA) or perform non-drug assisted endotracheal intubation, confirming with ETCO2.
The Ceiling (Page 11 Fork): If patient has trismus, clenching, or reactive airway reflexes, forcing an airway causes severe laryngospasm, hypoxia, and fatal ICP spikes. RSI is marked as ~ Purple text ~ (~ECP~ ONLY).
🚨 ILS/*ECT* Backup Trigger: Patient needs definitive airway protection but has active muscle tone or trismus. Action: Maintain gentle oxygenation via BVM, position lateral if vomiting, and request ~ECP~ intercept for pharmacological RSI.
The Trismus and Reflex Trap
Insert an OPA into an agitated, trismic brain-injured casualty with active airway reflexes precipitates massive emesis and laryngospasm. An OPA offers ZERO protection against aspiration. Consider a NPA if midface is intact or escalate immediately to definitive ALS airway.
Emergency Care Practitioner (ECP / ALS Scope)
Execution (Pages 12–15): Executes full pre-hospital Rapid Sequence Intubation (RSI):
Hemodynamic Pre-Optimization: Administers push-dose Adrenaline (5–20 mcg) to raise MAP ≥ 65 mmHg prior to induction, preventing post-induction cardiac arrest.
Neuroprotection: Administers Fentanyl (3 mcg/kg slow IV, Page 14) to blunt the sympathomimetic reflex spike in intracranial pressure caused by direct laryngoscopy.
Induction & Paralysis: Administers reduced-dose Ketamine (1 mg/kg) or Etomidate (0.2 mg/kg), followed immediately by Rocuronium (1.2 mg/kg IV, Page 13).
Intubation & Verification: Passes cuffed ETT smoothly using a gum elastic bougie; confirms placement immediately with continuous quantitative waveform ETCO2 (35–45 mmHg).
Ketamine Hydrochloride(Dissociative Anesthetic (Ketalar))
Advanced & Specialist Cadres (ANT / ECP Scope)
CDST P. 6, 8, 9 & 28Tactical field execution
Emergency Care Practitioner (ECP / ALS Scope)
Execution (CDST Page 18): Connect patient to transport mechanical ventilator on lung-protective settings:
Tidal Volume: 6–8 mL/kg Ideal Body Weight (IBW).
Ventilator Rate: 12–15 breaths per minute.
PEEP: 5 cmH2O | Target Saturation: 94–98%.
Target ETCO2: Strictly maintained between 35–45 mmHg (4.6–6.0 kPa).
Post-Intubation Maintenance (Page 16 & 19): In hemodynamically unstable trauma, run continuous Ketamine (0.25–0.5 mg/kg/hr) + Midazolam (0.05 mg/kg/hr) IV infusion.
The "Two-Handed" Jaw Thrust for Bumpy Roads
Defeating Trismus without Inducing "The Vomit Volcano"
The "Finger Tapping" Cadence to Stop Hyperventilation
WHY BAGGING TOO FAST KILLS
Why Hyperventilation Kills the Injured Brain? 1. The Chemistry (The Trigger): Hyperventilation blows off carbon dioxide (CO2) through the lungs faster than the body produces it. As blood levels of CO2 drop (ETCO2 < 35 mmHg), the blood and cerebrospinal fluid (CSF) become alkalotic (respiratory alkalosis—a rapid rise in pH). 2. The Vascular Response (The Reaction): Cerebral blood vessels are chemically sensitive to CO2 and pH levels: High CO2 (Acidosis): Dilates cerebral vessels, increasing intracranial blood volume and spiking intracranial pressure (ICP). Low CO2 (Alkalosis): Triggers immediate, aggressive cerebral vasoconstriction—the brain’s arterial blood vessels clamp shut. 3. The Clinical Consequence (The Ischemic Trap): When cerebral arterioles constrict, Cerebral Blood Flow (CBF) plummets by 30% to 50%. In an already injured, contused, or swollen brain (TBI), this sudden drop in perfusion starves vulnerable brain tissue (the penumbra) of vital oxygen and glucose. You induce severe secondary cerebral ischemia and irreversible brain tissue death, even while your pulse oximeter shows 100% SpO2.
• Bagging too fast → Low ETCO2 (< 35 mmHg) → Vessels clamp shut → Brain starves of oxygen (Ischemia / Infarction). Bagging too slow → High ETCO2 (> 45 mmHg) → Vessels dilate wide → Intracranial pressure spikes (Brainstem Herniation) The Target: Maintain quantitative ETCO2 strictly between 35 and 45 mmHg at all times!
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Disclaimer: This guide is for peer discussion and educational scenario simulation only. It does not replace individual clinical judgment, statutory protocols, or local clinical governance. All images featured in this document are AI-generated conceptual illustrations and do not depict real persons, patients, or actual scenes. Not an official publication of the HPCSA or UCT.
Author: Jacoline (Jax) Geldenhuys, BEMCHPCSA Registered Emergency Care Practitioner (ECP) since 2018(Registration and credentials verified on the official HPCSA public portal)© 2026 Paramedic Cases: SA EMS Field Protocols. All rights reserved.
This digital clinical companion is an independent educational and decision-support reference. All clinical algorithms reflect the HPCSA PBEC Clinical Decision Support Tools (CDST Version 1.3, October 2025), read in direct conjunction with the HPCSA List of Capabilities and Medications (Annexure A, April 2022) and the parent Clinical Practice Guidelines (2018).
Clinical Accountability: Per HPCSA Ethical Guidelines (Booklet 20), digital and algorithmic tools serve strictly as an adjunct to professional judgment. This platform does not provide automated diagnostic prescription. Registered practitioners are legally bound to verify all medication dosages, contraindications, and procedural scopes against their registered HPCSA scope of practice and local provincial clinical governance frameworks.
